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PAS 506 > Exam 5 (GI Tract) > Flashcards

Exam 5 (GI Tract) Flashcards

1
Q

What organ does most of absorption

A

Small intestine

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2
Q

Immune defenses of GI tract

A

Low pH of stomach.
Intestinal luminal bacteria.
Mucosa-associated lymphoid tissue (MALT) like Peyer’s patches have T cells and B cells

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3
Q

Parasympathetic actions on GI tract

A

vagus and pelvic nerves
increase smooth muscle activities
Relax sphincters

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4
Q

Sympathetic actions on GI tract

A

Celiac and mesenteric ganglia.
Decrease motility.
Causes sphincters to contract.
Inhibits secretion of digestive enzymes

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5
Q

Hirschsprung disease

A

missing part of myenteric plexus usually in large intestine.
Causes spasm of affected segment.
Causes stool to fill afffected segment.

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6
Q

What neurotransmitter is generated in submucosal plexus

A

Acetylcholine

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7
Q

What would cholinergic medications cause

A

Cramping and diarrhea

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8
Q

What would anticholinergic medications cause

A

Dry mouth and constipation

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9
Q

What are the three salivary glands of mouth

A

Parotid
Submandibular
Sublingual

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10
Q

Amylase

A

In saliva
Breaks down starch.
Also released from pancreas exocrine

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11
Q

Lingual Lipase

A

In saliva
Breaks down fats

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12
Q

ph of saliva

A

7.0

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13
Q

When is saliva production inhibited

A

Sleep
Fear

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14
Q

What starts peristaltic activity in esophagus

A

Distension of esophagus (spreading of esophagus causes it to contract to move food towards stomach.)

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15
Q

What part of nervous system controls peristalsis and sphincter tone

A

Enteric nervous system

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16
Q

What part of nervous system is the upper esophagus

A

extrinsic nervous system

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17
Q

Cardia

A

Accepts food from esophagus

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18
Q

Fundus

A

Where food collects in stomach

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19
Q

Body of stomach

A

Where food is churned and mixed

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20
Q

Pylorus

A

Releases food from stomach into duodenum

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21
Q

Ruggae

A

Folds of stomach to increase surface area

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22
Q

Surface cells of stomach secretions

A

Bicarbonate
Mucus

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23
Q

Parietal cells of stomach secretions

A

HCl
Intrinsic factor

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24
Q

Intrinsic factor

A

Secreted by parietal cells of stomach
Binds to vitamin B12 in stomach

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25
Q

Chief cells of stomach secretions

A

Pepsinogen
Gastric lipase

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26
Q

Enterochromaffin-like (ECL) cells of stomach

A

Secrete histamine

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27
Q

G cells of stomach

A

Secrete gastrin in response to peptides

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28
Q

Gastrin

A

Secreted by G-cells of antrum of stomach and duodenum
Stimulate parietal cells to make HCL
Stimulated in response to peptides.
Negative feedback by low pH

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29
Q

D-cells of stomach

A

Secrete somatostatin in response to acid in lumen.

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30
Q

Somatostatin

A

Secreted by D-cells of stomach
Stimulated to response to acid in lumen
Inhibits acid secretion
Inhibit gastrin release
Inhibit histamine release
Turns everything off (party pooper)

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31
Q

Proton Pump Inhibitors

A

Medicine that binds irreversibly to H+/K+ pump pf parietal cells to inhibit the secretion of H+

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32
Q

What all does the vagus nerve stimulate to happen in stomach

A

Acid secretion from parietal cells.
Histamine secretion from ECL cells

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33
Q

What does gastrin stimulate in stomach

A

Histamine release form ECL cells that then directly stimulates parietal cells to make HCl

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34
Q

List small intestine parts proximal to distal

A

Duodenum
Jejunum
Illeum
(DJ Illeum🎧🎶💿🎹)

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35
Q

Microvilli

A

Cillia of epithelium of small intestine to increase surface area. Helps form the brush border

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36
Q

Brush border of small intestine

A

Microvilli
Villi
Crypts
Paneth cells
Goblet cells
Digestive enzymes

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37
Q

Intestinal crypt

A

Small valleys next to villi of small intestine to make even more surface area

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38
Q

Goblet cells

A

Secret mucus in small intestine

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39
Q

Paneth cells

A

secrete antimicrobial peptides

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40
Q

CCK

A

Cholecystokinin.
Relaxes Sphincter of Oddi and causes gallbladder t contract to secrete bile into duodenum of small intestine.
Also promotes secretion of digestive enzymes of the pancreas into the duodenum

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41
Q

Secretin

A

Produced in duodenum in response to acid in duodenum.
Increases bicarbonate production from pancrease

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42
Q

Gastric inhibitory peptide

A

Produced in duodenum and jejunim in response to glucose and fat in duodenum.
Stimulates insulin secretion

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43
Q

Vasointestinal Peptide

A

Neurotransmitter.
Stimulates intestinal secretion of electroyltes and water.

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44
Q

Motilin

A

Secreted by ECL cells in stomach, small intestine, and colon.
Induces smooth muscle contraction between meals

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45
Q

Serotonin

A

Secreted by ECL cells of brush border in response to distention of gut wall.
Mostly excitatory and increases GI motility

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46
Q

Neuroendocrine carcinoid tumor

A

Causes oversecretion of serotonin.
Causes flushing, diarrheaa, bronchospasm, cardiac valvular disease.
Somatostatin used to help symptoms by decreasing release of serotonin

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47
Q

Breakdown of starch

A

Salivary and pancreatic amylase convert it to oligosaccharides.
Enzymes of luminal wall of intestines break down oligosaccharides and disacharides

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48
Q

Breakdown of protein

A

Pepsin in stomach.
Then pancreatic elastase, trypsin, and chymotrypsin

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49
Q

Breakdown of fat

A

Lipases from mouth, stomach and pancreas.
Emulsion formation with bile

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50
Q

What all is absorbed in small intestine and how

A

Monosaccharides via Na-coupled cotransport and diffusion.
Amino acids via sodium or hydrogen coupled transporters.
Lipds via transport proteins as long-chain fatty acids

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51
Q

Where does most fluid absorption of food happen

A

ascending colon.

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52
Q

Jobs of large intestine

A

Fluid absorption.
Bacterial fermentation
Production of vitamin K
Deconjugation of bile acid to return to portal circulation.
Fermentation of fiber into short chain fatty acids.
Storage and elimination of waste

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53
Q

Haustra

A

Segments of large intestine.
More active on left side to slow down feces before excretion.
(Pump the breaks I’m about to shit myself)

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54
Q

Largest organ in body (besides skin)

A

Liver

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55
Q

Primary functions of liver

A

Filtration and storage of blood.
Metabolism.
Detoxification.
Plasma protein production.
Bile formation.
Bilirubin metabolism.
Regeneration (regenerates itself)

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56
Q

Hepatic lobules

A

Basic functional unit of liver

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57
Q

Hepatocytes

A

Liver cells.
80% of liver mass.
Produce bile
Synthesize proteins.
Metabolize carbs, lipids, proteins, drugs.
Detoxify substances.
Store vitamins, minerals, and glycogen.

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58
Q

Sinusoids

A

Capillaries in lobules of liver.
Lined with Kupffer cells.
Filter blood.
Immune response.
Have stellate (Ito) cells

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59
Q

Kupffer cells

A

In sinusoids of liver
Macrophages of liver

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60
Q

Stellate (Ito) cells

A

In sinusoids of liver
Store vitamin A.
Play roles in fibrosis and regulation of blood flow

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61
Q

Bile canaliculi

A

Small ducts between hepatocytes that collect bile.
Merge to form bile ducts.

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62
Q

Connective tissue of liver

A

Separates lobules to keep everything compartmentalized and gives structure

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63
Q

Portal vein system

A

Carries blood from GI tract to liver to be filtered.
Blood then goes through hepatic veins and into inferior vena cava

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64
Q

Liver job in carb metabolism

A

Glycogen storage when blood sugar high.
Gluconeogenesis when blood sugar low

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65
Q

Liver job in lipid metabolism

A

Stores and makes lipids.
Ketogenesis

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66
Q

Ketogenesis

A

Converts fatty acids to ketone bodies for energy

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67
Q

Protein metabolism in liver

A

Synthesis of plasma proteins.
Amino acid metabolism
Amonia detoxification.

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68
Q

Amonia detoxification in liver

A

Turns amonia from breakdown of amino acid into urea to be pissed out.

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69
Q

What plasma proteins does the liver synthesize

A

ALBUMIN
Clotting factors
Lipoproteins

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70
Q

What regulates the fed state and what happens

A

INSULIN helps glucose enter cell and liver will stor glucose, make energy or make fat.

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71
Q

What regulates the fasting state and what happens

A

GLUCAGON, epinephrine, and cortisol
Glycogenolysis to put glucose into blood.
Gluconeogenesis

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72
Q

Lipoproteins

A

Transport lipids in circulation

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73
Q

Cholesterol

A

Made in liver.
Precursor for steroid hormones.
Cell membrane component.
Converted into bile acids/salts
Excess removed through bile

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74
Q

Protein metabolism

A

Steak –> proteins–> AA–> absorbed into blood –> liver ant tissue.
Can be turned into enzymes, hormones, glucose, or fatty acids

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75
Q

Nonessential AA

A

formed by liver

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76
Q

Albumin

A

Most common plasma protein.
Made by liver.
Maintains oncotic pressure.
Transports stuff in blood

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77
Q

Transport proteins made by liver

A

Transferrin (iron)
Ceruplasmin
Haptoglobin (eat RBC fragments)
Thyroxine binding globulin

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78
Q

Clotting factors made by liver

A

I, II, V, XII, IX, X, XI, XII, XIII.
Protein C and S.
Antithrombin.
Many vitamin K dependent

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79
Q

Acute phase proteins made by liver

A

Respond to inflammation.
CRP
Serum amyloid A
Fibrinogen
Alpha-1 antitrypsin.
Haptoglobin.
Ferritin.

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80
Q

Binding proteins made by liver

A

Sex hormone binding globulin.
Corticosteroid binding globulin.

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81
Q

Enzymes made by liver.

A

AST/ALT used in AA metabolism.
Angiotensinogen

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82
Q

Proteins made by liver

A

Albumin
Clotting factors
Transport proteins
Acute phase proteins
Complement
Binding proteins
Enzymes

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83
Q

Lipoproteins made by liver

A

VLDL
HDL

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84
Q

VLDL

A

Very low density lipoproteins.
Transport triglycerides from liver to peripheral tissues.
Converted to IDL in bloodstream and to LDL in liver.

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85
Q

HDL

A

High density lipoproteins.
Reverse cholesterol transport (from tissues back to liver)

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86
Q

Hormones made by liver

A

IGF-1
Thrombopoietin
Hepcidin for iron absorption
Ferroportin transports iron out of cell

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87
Q

Storage protein made by liver

A

Ferritin
Ceruplasmin

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88
Q

Phase I rxn of liver

A

Cytochrome P450 enzymes catalyze hydroxylation rxns to make drug more water soluble

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89
Q

Phase II rxn of liver

A

Conjugation of hydrophilic substance onto drug to make it more water soluble.

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90
Q

Phase III rxn of liver

A

Transport of substrate into either bile or blood for excretion

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91
Q

What is billirubin made of

A

80% Broken down hemoglobin and 20% turnover of heme from other tissues

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92
Q

Billirubin metabolism

A

Unconjugated (indirect) billirubin turned into conjugated (direct)

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93
Q

Bile

A

Made by liver and stored in gallbladder to be released into duodenum.
Used for digestion and absorption of fats and fat-soluble vitamins (ADEK) in small intestine.

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94
Q

What makes up bile

A

Bile salts
Bile acids
Phospholipids
Cholesterol
Bilirubin
Electrolytes

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95
Q

Sphincter of Oddi

A

Sphincter between liver/gallbladder and duodenum of small intestine.
Also controls flow of pancreatic juice into duodenum

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96
Q

What nutrients does the liver store

A

Glycogen.
Vitamins ADEK and B12
Iron
Copper

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97
Q

What hormones are metabolized in liver

A

ESTROGEN (makes guys have tits if not metabolized)
Insulin
Glucagon
Cortisol

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98
Q

What hormones are secreted or activated by liver

A

IGF-1
Hepcidin
Vitamin D
T4–>T3

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99
Q

Alanine aminotransferase (ALT)

A

Liver enzyme
Mostly in hepatocytes.
Assist gluconeogenesis and AA metabolism.
Hepatocyte injury puts ALT into blood

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100
Q

Aspartate Aminotransferase (AST)

A

Liver enzyme
Assist urea cycle and AA metabolism in hepatocytes.
Hepatocyte injury puts AST into blood.

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101
Q

How can a hepatocyte injury be seen in lab blood work

A

ALT and AST will be elevated

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102
Q

Alkaline phosphatase (ALP)

A

Liver enzyme
Increases concentration in bile ducts, liver, bones, and placenta.
Removes phosphate groups from various molecules.
Increased levels in blood indicate ductal damage (cholestasis, liver damage, bone damage.

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103
Q

Gamma-Glutamyl Transferase

A

Liver enzyme.
“Another ALP”
Does metabolism of glutathione in bile ducts, liver, and kidneys.
Increased levels in blood indicate bile duct disfunction/cholestasis as well as alcohol use

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104
Q

Lactate dehydrogenase

A

Liver enzyme.
found everywhere.

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105
Q

Cholestasis

A

Reduction or stop of bile flow

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106
Q

Where does bile flow when sphincter of Oddi is closed

A

Gallbladder

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107
Q

Where does bile flow when sphincter of Oddi is open

A

Duodenum of small intestine

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108
Q

Function of gallbladder

A

Store and concentrate bile.
Concentrated 3-10 fold by removal of water and electrolytes

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109
Q

What determines if bile goes into gallbladder or duodenum from liver

A

Pressure of gallbladder, liver, and sphincter of Oddi.
It will always flow from high to low pressure

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110
Q

How much bile reenters portal vein to return to liver

A

95%

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111
Q

How much bile released from gallbladder is excreted in feces

A

5%

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112
Q

Exocrine part of pancreas

A

Acinar cells

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113
Q

Endocrine part of pancreas

A

Islets of Langerhans

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114
Q

Islet of langerhans

A

Endocrine part of pancreas.
All throughout pancreas.
More common in tail than head or body.
Secrete glucagon (alpha) insulin (beta), somatostatin (delta), pancreatic peptide (F)

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115
Q

Insulin

A

Secreted by beta cells of pancreas.
Anabolic.
Increases the storage of glucose, fatty acids, and amino acids.
Lowers blood sugar by inhibiting gluconeogenesis, glycogenolysis, and lipolysis.
Stimulated by high blood sugar.
Promotes, glucose uptake by cells, glycogenesis, lipogenesis, protein synthesis

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116
Q

Glucagon

A

Secreted by alpha cells of pancreas.
Catabolic.
Mobilizes glucose, fatty acids, and amino acids into blood stream.
Raises blood sugar by stimulating glycogenolysis, gluconeogenesis, and lipolysis
Stimulated by low blood sugar

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117
Q

How does glucose get into B cell

A

GLUT transporters

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118
Q

Calcium

A

Makes stuff happen.
Pulls the trigger on everything

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119
Q

Insulin synthesis

A

Made in rough ER of B cell.
Transported to golgi.
Packaged into membrane-bound granules.
Granules move to plasma membrane for exocytsis.
Crosses over capillary endothelium into blood stream and acts quickly

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120
Q

Half life of insulin

A

5 mins. (very short)

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121
Q

Is secretion of insulin part of sympathetic or parasympathetic

A

Parasympathetic

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122
Q

Insulin relationship with potassium

A

Insulin causes K to enter cell causing extracellular K to decrease.
So pts with insulin infusions often develop hypokalemia

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123
Q

Type 1 diabetes

A

Autoimmune destruction of beta cells

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124
Q

Type 2 diabetes

A

Dysregulation of insulin release from B cells and increases of insulin resistance of peripheral tissue.
Leads to eventual B cell death

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125
Q

Effects of hyperglycemia

A

Hyperosmolality of blood.
Glucose spills out into blood.
Water follows glucose causing water loss, dehydration, polydipsia

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126
Q

Exocrine function of pancreas

A

Produces 1.5 liters of digestive enzymes.
Amylase
Protease
Lipase
Carboxypeptidase
Ribonuclease
Deoxyribonuclease
Phospholipase A
Trypsinogen
Chymotrypsinogen
Procarboxypolypeptidase

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127
Q

Trypsin

A

Activates everything.
So converting trypsinogen (made by pancreas, exocrine) into active form trypsin gets everything going

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128
Q

Zymogen

A

Inactive form of enzyme

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129
Q

Maltase

A

Breaks maltose into two glucose

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130
Q

Sucrase

A

Breaks sucrose into glucose and fructose

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131
Q

Lactase

A

Breaks down lactose into glucose and galactalose

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132
Q

What stimulates release of CCK

A

Fatty acids and Amino acids

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133
Q

Where is vitamin B12 absorbed

A

Illeum but must be bound with intrinsic factor from parietal cells of stomach

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134
Q

What BMI is overweight

A

25-29.9

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135
Q

What BMI is underweight

A

<18.5

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136
Q

What is a healthy BMI

A

18.5-24.9

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137
Q

BMI for Obesity class 1

A

30-34.9

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138
Q

BMI for Obesity Class 2

A

35-39.9

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139
Q

BMI for Morbid Obesity

A

> 40

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140
Q

What waist length is related to increased risk of diabetes, HTN, CAD

A

> 35 inches in women
40 inches in men

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141
Q

Where to measure waiste circumference

A

Uppermost point on iliac crest

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142
Q

What waist to hip ratio is increased risk for weight related problems in men

A

> 1.0

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143
Q

What waist to hip ratio is increased risk for wait related problems in women

A

> 0.85

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144
Q

Estimated Average Requirement (EAR) of dietary intake

A

Indicator of adequacy to meet needs of half of the healthy individuals in a life stage

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145
Q

Recommended Daily Allowance (RDA) of dietary intake

A

Average requirement plus two standard deviations. Established to prevent deficiency in healthy people, not inhance health

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146
Q

Adequate intake (AI)

A

Estimated intake of healthy population

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147
Q

Tolerable Upper Limit (TUL) of dietary intake

A

Upper limit unlikely to pose a risk of adverse health effects.

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148
Q

Steps of nutritional therapy

A

Evaluate
Assess
Determine
Monitor
Validate

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149
Q

Carbohydrates

A

4kcal/g
50-60% calorie intake
main source of energy
Stored as glycogen in liver and muscle
Enhance learning and memory

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150
Q

Proteins

A

4 kcal/g
About 20% calorie intake.
Need about 1g/kg per day
SUpport muscle mass
Used in cell walls, enzymes, hormones peptides, antibodies.
Fuel source

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151
Q

Fats

A

9 kcal/gram
Main source of energy STORAGE/adiposity
Vehicle for fat soluble vitamins
Makes up cell membranes and hormones
Source of essential fatty acids
Less than 30% calorie intake
Makes food taste good and you feel full

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152
Q

Fiber

A

Should get 25g per day
Usually we only get like 10

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153
Q

Essential amino acids

A

Must be eaten bc we can’t make them.
PVT TIM HLL
Phenylalanine
Valine
Threonine
Tryptophan
Isoleucine
Methionine
Histidine
Leucine
Lysine

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154
Q

Positive nitrogen balance

A

Indicates an anabolic state

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155
Q

Negative nitrogen balance

A

Indicates a catabolic state.

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156
Q

Ideal Nitrogen balance

A

+1-+4

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157
Q

What controls apetite

A

Hypothalamus

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158
Q

Limbic system role in apetite

A

Controls reward and motivation.
Plays role in addition

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159
Q

Neural connection between gut and brain

A

Vagus nerve

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160
Q

Ghrelin

A

Made in stomach
Stimulates appetite in response to no food.
Promotes weight gain.
Acts on hypothalamus

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161
Q

What surgery reduces ghrelin levels

A

Gastric bypass surgery

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162
Q

Leptin

A

Made in adipocytes.
Acts on hypothalamus to decrease appetite in feedback mechanism.
Signals adequate energy stores in puberty.
Stimulates sympathetic nervous system to use energy.
Leptin resistance could be linked to leptin

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163
Q

Glucagon Like peptide (GLP-1)

A

Made by intestinal L-cells
Antagonizes CB1 receptors causing decreased feeding, weight loss, incretin effect on insulin secretion.
Used to treat diabetes and obesity

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164
Q

Peptide YY

A

Released by jejunum in response to fat
Decreases food intake
Inhibits gastric acid secretion.
Inhibits stomach motility.

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165
Q

Oxyntomodulin

A

Induces satiety.
Increases energy expendature.
Decreases weight.

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166
Q

Adiponectin

A

Secreted by adipocytes in response to fasting.
Makes cells more sensitive to insulin and increases fatty acid oxidation.
Decreases visceral fat mass.

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167
Q

List of macrominerals (major minerals)

A

Calcium
Chloride
Phosphorus
Potassium
Sulfur
Sodium
Magnesium

168
Q

Sodium function

A

Maintain fluid balance.
Maintain acid-base balance
Nerve, muscular impulse conduction

169
Q

Sodium deficiency

A

Hyponatremia.
Headache
seizure
encephalopathy
Muscle twitching

170
Q

Sodium toxicity

A

Hypernatremia
Agitation
Coma

171
Q

Sodium supplementation

A

Needed in excess sweat.
Needed in addison’s disease

172
Q

Potassium function

A

Conduction of nerve impulses
Muscle contractions

173
Q

Potassium deficiency

A

Hypokalemia
Weakness
Diminished reflexes
paresthesia
Arrhythmia

174
Q

Potassium toxicity

A

Hyperkalemia
Seen in renal failure.
Abdominal cramping
Arrhythmia
Cardiac arrest

175
Q

Potassium supplementation

A

Only for accelerated losses

176
Q

Calcium function

A

Bone mineralization.
Muscle contraction
Blood clotting

177
Q

Calcium deficiency

A

Hypocalcemia
Chronic is osteoperosis.
Acute is irritability, paresthesia, tetany, seizure

178
Q

Calcium toxicity

A

Seen in hyperparathyroidism and cancers

179
Q

Calcium supplementation

A

Calcium citrate more easily absorbed bc more acidic but calcium carbonate has more calcium

180
Q

Phosphorus function

A

In bones and teeth.
DNA
RNA
ATP
ADP

181
Q

Phosphorus deficiency

A

Bone loss
Muscle weakness
Refeeding syndrome

182
Q

Phosphorus toxicity

A

Renal disease.
Treated with phosphate binders to stop absorption

183
Q

Phosphorus supplementation

A

None

184
Q

Iron function

A

Oxygen delivery
In hemoglobin, myoglobin, and cytochromes

185
Q

Iron deficiency

A

Weakness, fatigue, SOB, microcytic anemia.
Developmental delays
Pallor
Clubbed nails

186
Q

Iron toxicity

A

Liver failure (first organ effected)
Hemochromatosis.

187
Q

Iron supplementation

A

Iron sulfate.
IV dextran.
Injectafer )ferric carboxymaltose

188
Q

Iodine function

A

Synthesis of thyroid hormone

189
Q

Iodine deficiency

A

Cretinism
Goiter

190
Q

Iodine toxicity

A

Acne
Goiter
Thyroiditis

191
Q

Iodine supplementation

A

None in US bc we have iodized salt

192
Q

Fluoride function

A

Protects teeth against dental carries.
Bone mineralization

193
Q

Fluoride deficiency

A

lack of fluoride in water sources

194
Q

Fluoride toxicity

A

Can disrupt tooth enamel

195
Q

Fluoride supplementation

A

Water supply
Tooth paste
Get it painted on teeth at dentist

196
Q

Zinc function

A

Component of enzymes, DNA, RNA
Collagen formation
Immunity

197
Q

Zinc deficiency

A

Growth retardation
Alopecia
Eczema
Loss of taste
Impaired immunity

198
Q

Zinc toxicity

A

Metallic taste
Anosmia
Inhibits copper absorption

199
Q

Zinc supplementation

A

In cold lozenges

200
Q

Fat soluble vitamins

A

ADEK

201
Q

Vitamin A function

A

Development and maintenance of mucus membranes and skin.
Plays role in vision and gonad function

202
Q

Vitamin A deficiency

A

Hyperkeratosis.
Night blindness.
Xeropthalmia

203
Q

Vitamin A toxicity

A

Tetratogenic acne medicine

204
Q

Vitamin A supplementation

A

Not reccomended bc caould increase cancers

205
Q

Vitamin D Function

A

Calcium phosphorus regulation.
Immunity.
Neuromuscular function

206
Q

Vitamin D deficiency

A

Rickets.
Osteomalacia.

207
Q

Vitamin D toxicity

A

Rare

208
Q

Calcitriol

A

Active form of vitamin D from kidney

209
Q

Calcidiol

A

Inactive form of vitamin D from liver

210
Q

Vitamin D supplementation

A

D2 from food
D3 from sun

211
Q

Vitamin E functino

A

Antioxidant.
Inhibits platelet aggregation

212
Q

Vitamin E deficiency

A

Rare.
Muscle weakness and weak immune system

213
Q

Vitamin E toxicity

A

Interfere with vitamin K formation of clotting factors

214
Q

Vitamin E supplementation

A

Roles in heart disease and cancer

215
Q

Vitamin K function

A

Cofactor for enzymes required for coagulation factors

216
Q

Vitamin K deficiency

A

Bruising
Mucosal bleeding
Melena
Hematuria

217
Q

Vitamin K toxicity

A

No TUL
Person on warfarin needs consistent daily dose

218
Q

Vitamin K supplementation

A

Infants given injections at birth.
Sometimes used therapeutically for warfarin overdose.

219
Q

Vitamin C (ascorbic acid) function

A

Antioxidant
Collagen formation.
Aids in iron reabsorption

220
Q

Vitamin C (ascorbic acid) deficiency

A

Scurvy
Seen in smokers, alcoholics, and pirates.
Elderly risk due to lack of fruits and vegetables

221
Q

Vitamin C (ascorbic acid) toxicity

A

NVD
Abdominal pain

222
Q

Vitamin C (ascorbic acid) supplementation

A

Used as antioxidant
Treat cold

223
Q

Vitamin B1 (thiamin) function

A

Essential for enzymes of energy production

224
Q

Vitamin B1 (thiamin) deficiency

A

Primary is Beriberi.
Impaired absorption is Wenicke’s encephalopathy.
Poor appetite, irritability, apathy, confusion, weight loss, clonus, neuropathy

225
Q

Vitamin B1 (thiamin) toxicity

A

None

226
Q

Vitamin B1 (thiamin) supplementation

A

In fortified grains.
Given in IV when treating alcoholic

227
Q

Vitamin B3 (niacin) function

A

DNA synthesis
Energy metabollsim
Skin, GI tract, Nervous system

228
Q

Vitamin B3 (niacin) deficiency

A

Pellegra
4Ds: diarrhea, dermatitis, dementia, death
Found in corn based diets

229
Q

Vitamin B3 (niacin) toxicity

A

Flushing and dizziness.
Major adverse cardiac events

230
Q

Vitamin B3 (niacin) supplementation

A

Made from tryptophan so usually don’t need supplements

231
Q

Vitamin B5 (pantothenic acid) function

A

Assist in fatty acid synthesis via coenzyme A

232
Q

Vitamin B5 (pantothenic acid) deficiency

A

Burning feet syndrome

233
Q

Vitamin B5 (pantothenic acid) toxcity

A

none

234
Q

Vitamin B5 (pantothenic acid) supplementation

A

Not needed in healthy adults.
Can get from eating eggs.

235
Q

Vitamin B6 (pyridoxine) function

A

Coenzyme in metabolism of amino acids
Treat pregnancy associated nausea.

236
Q

Vitamin B6 (pyroxidine) deficiency

A

Glossitis
Cheilosis
Dermatits
Neuropathy

237
Q

Vitamin B6 (pyridoxine) toxicity

A

Neuropathy
blindness

238
Q

Vitamin B9 (folic acid) function

A

Essential for formation of DNA RNA heme.
Conversion of homocysteine to methionine

239
Q

Vitamin B9 (folic acid) deficiency

A

Neural tube defects

240
Q

Vitamin B9 (folic acid) Toxicity

A

Can make B12 deficiency

241
Q

Vitamin B12 (Cobalamin) function

A

Cell replication and neurologic function

242
Q

Vitamin B12 (cobalamin) deficiency

A

Megaloblastic anemia.
Pernicious anemia.
Neuropathy.
Seen in vegetarians and elderly

243
Q

Vitamin B12 (cobalamin) toxicity

A

not documented

244
Q

Vitamin B 12 (cobalamin) supplementation

A

From Animal sources.

245
Q

Pernicious anemia

A

Lack of intrinsic factor.
Can cause deficiency of B12

246
Q

Biotin function

A

Coenzyme in synthesis of fat, glycogen, and amino acids

247
Q

Biotin deficiency

A

Alopecia
Dermatiis
Paresthesia

248
Q

Biotin toxicity

A

Rare
Can interfere withs some lab tests like troponin

249
Q

Biotin supplementation

A

Usually not needed

250
Q

Peptide hormones

A

Pancreas
Pituitary
Parathyroid
Gastrointestinal
Made as prohormones
Active hormones stored in intracellular vesicles
Mostly water soluble so don’t require carrier molecules in blood

251
Q

Amine hormones

A

Catecholamines and thyroidd hormones.
Tyrosine based
Catecholamines are water soluble.
Thyroid hormones not water soluble so need carrier protein in blood

252
Q

Steroid hormones

A

Made from cholesterol
Rapidly diffuse once synthesized due to high lipid solubility.
Needs carrier protien in blood

253
Q

Primary disorder

A

Excess or deficiency of secretion by target gland

254
Q

Secondary disorder

A

Excess or deficiency of secretion by pituitary

255
Q

Tertiary disorders

A

Excess or deficiency of secretion by hypothalamus

256
Q

Dynamic/provacative hormone test

A

Measures changes in hormone levels in response to stimulus

257
Q

Hypothalamus jobs

A

Control HR, temp, appetite, thirst, sleep cycle

258
Q

Hypothalamic hormones

A

ADH
OT
CRH
TRH
GHRH
GHIH (somatostatin)
GnRH
PRH
Dopamine (prolactin inhibiting)

259
Q

Antidiuretic hormone (ADH) (Vasopressin)

A

Controls water Balance
Combats dehydration.
Release stimulated by decreased blood volume or increases in serum osmolality.
Stimulates thirst via hypothalamus

260
Q

ADH receptors

A

V1 in vascular smooth muscle
V2 in kidneys

260
Q
A
261
Q

Oxytocin (OT)

A

Stimulates uterine contraction in parturition in positive feedback mechanism.
Stimulates milk let down and ejection.
Promotes maternal and social bonding.
Prostate health and disease

262
Q

What hormones come from posterior pitutary

A

ADH
OT

263
Q

Prolactin

A

Controls milk production from ant pit

264
Q

How do hypothalamic hormones control release of ant pit hormones

A

Hypophhyseal portal blood supply
All ant pit hormones control release of other hormones except for PRL

265
Q

TSH

A

Thyroid stimulating hormone
Thyrotrope

266
Q

FSH

A

Follicle stimulating hormone
Gonadotroph

267
Q

LH

A

Lutenizing hormone
Gonadotroph

268
Q

ACTH

A

Adrenocorticotropic hormone
Corticotrope

269
Q

GH

A

Growth Hormone
Somatotroph

270
Q

PRL

A

Prolactin
Lactotroph

271
Q

PRL control

A

Inhibited by dopamine
Release stimulated by TRH and OT.
Levels rise after start of sleep and are lowest at midday.

272
Q

PRL actions

A

Lactogenesis/lactation
Breast development
sleep
Reproduction
Ovulation

273
Q

Most common secondary pituitary adenoma

A

Prolatinoma

274
Q

FSH/LH control

A

Negative feedback from testosterone, estrogen, inhibin

275
Q

FSH actions in men

A

Spermatogenesis in s in sertoli cells of testes which produce inhibin as negative feedback on FSH

276
Q

FSH actions in women

A

Increases estrogen production from ovaries

277
Q

LH actions in women

A

Induces ovulation in pulsatile fashion

278
Q

Progestins

A

Female sex steroid.
Prepare uterine endometrium
Increase as result of LH surge and supported by corpus luteum

279
Q

Estrogens

A

Female puberty
Menstrual cycle
Ovaries make greatest amount of estradiol

280
Q

Androgens

A

Main male sex steroids
Testosterone is main circulating androgen

281
Q

LH actions on men

A

Cause Leydig cells of testes to make testoasterone

282
Q

GH control

A

Somatostatin inhibits release.
GH released in early morning
Releases stimulated by GHRH, hypoglycemia, serum arginine concentration, hunger from grhelin

283
Q

GH actions

A

Stimulates growth of everything.
Stimulates secretion of IGF-1

284
Q

GH deficiency

A

If before puberty, small stature.
If after puberty, obesity, dyslipidemia, depression.

285
Q

Gigantism

A

GH excess before puberty

286
Q

Acromegaly

A

GH excess after puberty

287
Q

TH control

A

T3 and T4 negative feedback on hypothalamus and ant pit

288
Q

TH actions

A

Increases basal metabolic rate
Increases sodium potassium pump activity.
Increases expression of beta adrenergic receptors.
Causes goiter if excess.
Releases calcitonin in response to hypercalcemia via c-cells

289
Q

Hypothyroidism

A

Often autoimmune from thyroid peroxidase

290
Q

Hyperthyroidism

A

Can be caused by thyroid stimulating immunogloubulin or TSH receptor Ab (grave’s disease)

291
Q

Calcitonin

A

Released from C-cells.
Levels increase in response to high calcium levels in blood.
Lowers circulating calcium and phosphate levels.
Inhibits bone resorption.
Increases calcium excretion into urine.

292
Q

High calcitonin

A

Associated with medullary cancer of thyroid

293
Q

ACTH control of release

A

Stimulated by CRH from hypothalamus.
Highest levels in morning.
Negative feedback on CRH and ACTH from cortisol

294
Q

ACTH actions

A

Stimulates adrenal glands to release corticosteroids to regulate metabolism and immune response.
Weakly stimulates aldosterone secretion

295
Q

ACTH deficiency

A

Causes hypocortisolism (secondary addison’s disease).
Atrophy of flomerulosa, fasiculata, and reticularis
Cause deficiencies in glucocrticoids, adrenal anrogens, and mineralocorticoids

296
Q

What part of adrenal gland is long-term responses

A

Cortex

297
Q

What part of adrenal gland is immediate response

A

Medulla

298
Q

Zona glomerulosa

A

Releases aldosterone (mineralocorticoid) to increases blood volume through water and Na retension

299
Q

Zona fasciculata

A

Releases cortisol (glucocorticoid) for metabolic homeostasis and immunity

300
Q

Zona reticularis

A

Releases DHEA (androgens) for development of sex hormones

301
Q

Aldosterone control of release

A

Mineralocorticoid
RAAS (angiotensin II).
Hyperkalemia stimulates secretion.
ACTH weakly stimulates secretion

302
Q

Aldosterone actions

A

Tells kidney to conserve water and sodium and get rid of potassium.
Increases blood volume.
Increases BP.
Can result in hypokalemia

303
Q

Glucocorticoid control of release

A

Increases as result of stress.
Stimulatesd by ACTH from ant pit.

304
Q

Glucocorticoid actions

A

Raise blood sugar.
Immune function suppression.
Pain reduction (steroid shot)

304
Q

Glucocorticoid example

A

Cortisol

305
Q

Cushing disease

A

Hypercortisolism.
Usually ACTH dependent

306
Q

Addison’s disease

A

Cortisol difficiency

307
Q

Adrenal androgen (DHEA) control of release

A

Stimulated by ACTH of ant pit.
Come from zona reticularis

308
Q

Adrenal androgen (DHEA) actions

A

converted into estrogens in ovaries and testosterone in testes

309
Q

DHEA deficiency in women

A

Decreased libido and pubic hair thinning

310
Q

DHEA excess

A

Seen in congenital adrenal hyperplasia
Acne
Hirsutism
Virilization in women.

311
Q

Most common cause of primary adrenal insufficiency

A

Addison’s disease.
Autoimmune where antibodies destroy adrenal gland

312
Q

What is main causes of secondary adrenal insufficiency

A

prolonged exposure to glucocorticoid

313
Q

Catecholamine control of releases

A

Come from adrenal medulla
Activates by sympathetic nervous system.
Cortisol stimulates epinephrine synthesis.

314
Q

Catecholamine action

A

Increase cardiac output
Bronchodilation
Elevated blood glucose.

315
Q

Catecholamine examples

A

Epi
Norepi

316
Q

Glucocorticoid example

A

Cortisol

317
Q

Parathyroid Hormone release control

A

Secreted by parathyroid glands.
Stimulated by hypocalcemia and hyperphosphatemia.
Inhibited by vitamin B

318
Q

Parathyroid Hormone actions

A

Increase calcium and decreases phosphate.
Bone resorption of calcium into blood
Increases calcium absorption of intestine
Stimulate vitamin D synthesis at kidney

319
Q

Hyperparthyroidism.

A

Hypercalcemia
Makes pt go crazy
Bones
Stones
Moans
Groans
Psychiatric overtones

320
Q

Chvostek’s sign

A

Hypocalcemia.
Facial spasm from tapping gacial nerve anterior to ear

321
Q

Trousseau’s sign

A

Hypocalcemia.
Carpal spasm in response to occlusion of brachial

322
Q

What causes releases of amylin

A

Spikes in blood glucose

323
Q

Amylin actions

A

Slows gastric emptying.
Increases satiety.
Inhibits glucagon secretion.

324
Q

Muscarinic receptors on gastric glands

A

M1

325
Q

Muscarinic receptors on parietal cells

A

M3

326
Q

Heartburn/GERD meds

A

Antacids - mineral
H-2 receptor blockers - -dine
Proton pump inhibitor - -prazole

327
Q

Peptic ulcer disease meds

A

Bismuth-based quad therapyy
Mucosal protective agents

328
Q

Diarrhea meds

A

Opioid receptor antagonist
Antidiarrheal

329
Q

Constipation meds

A

Stool softner
Osmotic laxatives
Stimulant laxatives
Bulk laxatives

330
Q

What receptors stimulate H+/K+ pumps to pump acid into stomach

A

M3 - acetylcholine
H2- histamine
CCK-B - gastrin

331
Q

Prostaglandin E2 (PGE2)

A

Decreases gastric acid secretion
Increases bicarbonate from epithelial cells, production of mucus, cell turnover, blood flow

332
Q

GERD

A

Gastroesophagesal reflux disease.
Very frequent heartburn.
Esophageal sphincter isn’t tight enough

333
Q

Acid neutralizers/antacid

A

Magnesium hydroxide
Calcium carbonate
Reduce pepsin activity.
Quick relief

334
Q

Magnesium hydroxide

A

Antacid
Adverse effect is diarrhea.
Don’t use in pt with kidney problems

335
Q

Calcium carbonate

A

Antacid
Adverse effect is constipation
Good calcium supplement

336
Q

H-2 receptor blocker

A

-tidine
inhibit binding of histamine to parietal cells thus decreasing acid secretion.
Peaks in 1-3 hours
Very well tolerated

337
Q

H-2 receptor blocker uses

A

GERD
Peptic ulcer disease
Acute stress ulcers through IV

338
Q

Proton Pump Inhibitors (PPI)

A

-prazole
Prodrug
Superior to H-2 blockers in suppressing acid secretion and increasing peptic ulcer healing.
Enteric coating so it will survive acidity of stomach to be absorbed in small intestine
Heavy hitters

339
Q

Proton Pump Inhibitor (PPI) method of action

A

Irreversibly bind and deactivate to H/K+ pump in parietal cells

340
Q

Cimetidine

A

H-2 Receptor blocker
CYP 450 inhibitor (effects other drug metabolism)
Antiandrogenic effects

341
Q

PPI uses

A

GERD
Peptic ulcer
H. pylori
Used when things get bad

342
Q

Long term PPI use

A

Want to get them on an H-2 or something once healed bc of adverse effects.

343
Q

Peptic ulcer

A

Breaks lining os stomach or duodenum
Caused by H. pyolori and NSAIDS

344
Q

What is used to treat peptic uclers

A

PPI
H-2 blockers
Reduce intragastric activity

345
Q

H. pylori

A

Gram negative
Requires antibiotic treatment
Transmitted orally.
Degrades mucosa
Causes ulcers

346
Q

NSAID risks

A

Responsible for topical injury and effects.
Weak acids
If ulcer or opening in stomach/intestinal line they can cause problem.
Don’t cause opening themselves.
Decrease prostaglandin synthesis.
Thats why we take with food

347
Q

H. pylori treatment

A

Bismuth-based quadruple therapy:
PPI
2 antibiotics
Bismuth subsalicylate

348
Q

Non-H.pylori peptic ulcer disease treatment

A

PPI PO QD-BID to decrease acid secretion.
Antacid/acid neutralizer PRN.
Mucosal protective agentto protect while ulcer heals

349
Q

Mucosal protective agents

A

Coating agents
Prostaglandin

350
Q

Sucralfate

A

Coating agent to protect mucosa
Forms negatively charged gel that binds to positive proteins to adhere to epithelial cells while healing.
Doesn’t affect pH, just coats to protect while healing

351
Q

Sucralfate

A

Mucosal protective agent
Prevents stress ulcers and treats duodenal ulcer
No toxicity
Causes constipation

352
Q

Bismuth Subsalicylate (peptol bismol) as mucosal protective agent

A

Mucosal protective agent
Interacts with necrotic mucossal tissue and forms protective barrier to protect ulcer.
Inhibits pepsin and increases mucus to protect ulcer.
Stimulates secretion of PGE2 and bicarbonates.
Stops growth of H. pylori.
Black tongue and stool

353
Q

Misoprostol

A

Mucosal protective agent
Inhibits histamine action at H-2 receptor.
Prevent NSAID induced ulcer
No pregnancy

354
Q

Antimotility agents to fix diarrhea

A

Opioid receptor agonist

355
Q

Fluid electrolyte transport modification to fix diarrhea

A

Bismuth subsalicylate

356
Q

Opiod receptor agonist

A

For diarrhea
Loperamide
Diphenoxylate/atropine

357
Q

Opioid receptor agonist method of action

A

Activate presynaptic opioid receptors in enteric nervous system.
Blocks ACh release.
Anti-SLUDGE
Anti-parasympathetic

358
Q

Opioid receptor adverse effects

A

Toxic megacolon
So don’t give to pt if they have fever, severe abdominal pain, swollen abdomen

359
Q

Loperamide

A

Opioid receptor agonist
Doesn’t cross BBB unless abused.
For acute/travelers diarrhea

360
Q

Diphenoxylate/atropine

A

Opiod agonist.
Van cause headache, dry mouth, constipation
Atropine to discourage abuse
Controlled substance

361
Q

Bismuth subsalicylate as antidiarrheal

A

Short term use
Avoid in kidney issues

362
Q

How to prevent constipation

A

High fiber diet
fluid intake
Regular exercise
Don’t hold poop

363
Q

Docusate

A

Stool softener
Allows water to penetrate oil layer around poop to soften stool
More preventative care than treatment
good after labor or at initiation of opioids

364
Q

Cons of laxatives

A

Electrolyte imbalance in long term use.
Potential risk of dependency

365
Q

Osmotic laxative

A

Water soluble
Nonabsorbable
Softens stool
Increases stool volume
Increases perstalsis

366
Q

Polyethylene glycol (miralax)

A

Osmotic laxative
over the counter
Onset of action is 1-3 days

367
Q

Simulant laxatives

A

Senna
Bisacodyl
Cause more urgent BM than osmotic laxatives

368
Q

Senna

A

Stimulant laxative
Irritates luminal sensory nerves stimulating colonic motility and reducing colonic water reabsorption.

369
Q

Bisacodyl

A

Stimulant laxatives
Prodrug converted in gut.
Increases water content of stool.
Expect BBM in 6-12 hours.

370
Q

Bulk laxatives

A

Form gels in large intestine causing water retension stimulating stretch receptors and increasing peristalsis.
Onset is 1-3 days
For mild constipation
CAN CAUSE INTESTINAL BLOCK if not enough water ingested
Decrease absorption of other meds so give at different time

371
Q

Methylcellulose

A

Bulk laxative
Less side effects

372
Q

Psyllium husks

A

Bulk laxative
Gas, bloating, abdominal cramping.
Good for getting everything out bc husks scrape the sides of colon

373
Q

ADH cellular effect on kidneys

A

Causes aquiporins to be expressed on cell membrane to take in water to then put back into blood rather than being excreted in urine

374
Q

How do we measure GH in blood

A

IGF-1

375
Q

What thyroid hormone is more metabolically active (potent)

A

T3 but T4 is made more bc thats how the chemistry work
We turn T4 into T3 in periphery

376
Q

Rapid acting bolus meds

A

Insulin aspart
Insulin lispro
Insulin glulisine
Inhaled insuline
Done at meal time

377
Q

TH replacement

A

Liothyronine
Levothyroxine
Desiccated thyroid

378
Q

Agents for hypothyroidism

A

Thioamides
methimazole
propylthiouracil

379
Q

What allows glucose to get into cells

A

Insulin unlocks GLUT-4 transport proteins

380
Q

GLP-1

A

Glucose in intestine stimulates GLP-1 secretion GLP-1 binds to beta cells causing insulin to be released

381
Q

What type of receptors are insulin receptors and what does their activation cause

A

Tyrosine kinase
So causes phosphoryaltion cascade and downstream effects.
Activation moves GLUT-4 transporters to surface

382
Q

Basal insulin

A

Keeps glucose levels stable through fasting.
Always there no matter food

383
Q

Bolus insulin

A

Responds to rise in blood glucose after food intake

384
Q

How do we make insulin for injection

A

Recombinant DNA from bacteria

385
Q

Why do we give insulin SQ

A

Its a polypeptide so it would denature in the stomach

386
Q

Prandial

A

Insulin given around time of food

387
Q

Short acting bolus meds

A

Reg human insulin

388
Q

Intermediate Basal insulins

A

Insulin isophane suspension
Slow absorption longer duration

389
Q

Long acting insulin

A

Insulin glargine
Insulin detemir
Insulin degludec
Human insulin analog
No true peak
Last long time

390
Q

Insulin adverse effects

A

Hypoglycemia
Weight gain
Injection sight reaction

391
Q

Glucagon meds

A

Generi glucagon emergency kit
Baqsimi
Gvoke hypopen
Given when blood sugar gets very low

392
Q

Baqsimi

A

Glucagon nasal powder
Inhalation not required
More effective than glucagon
Easiest to use

393
Q

Gvoke Hypopen

A

Gluvaon autoinjector
Like an epipen for glucagon

394
Q

Meds that increase insuln secretion

A

Sulfonylureas
Glyburide
Glipizide
Glimepiride

395
Q

Sulfonylureas

A

G drugs
Cause insulin secretion
Block ATP sensitive K channel in beta cells causing depolarization and infulx of calcium causing insulin secretion.

396
Q

Glyburide

A

Sulfonylurea
Longest acting insulin secretion drug.
Greatest risk of hypoglycemia and weight gain.

397
Q

Drugs that increases glucose-dependent insulin secretion

A

Hypoglycemia not as big of a risk
GLP-1 receptor agonist
GIP receptor agonist
DPP-4 inhibitors

398
Q

Endogenous incretins

A

GLP-1
GIP
Secreted by gut after eating
Stimulate insulin secretion in response to high glucose
Inactivated by DPP-4

399
Q

GLP 1 receptor agonist drugs

A

-atide or -glutide
Bind to GLP-1 receptor on beta cell activating signaling cascade increasing adenylyl cyclase and cAMP causing insulin release

400
Q

GLP 1 receptor agonist adverse effects

A

-atide or -glutide
Box warning is thyroid c cell tumor risks

401
Q

Tirzepatide

A

GLP-1/GIP receptor agonist
Binds to both receptors increasing glucose dependent insulin release
“twincretin”
More effective
Box warning for c-celll tumor risk
effect hormonal birth control

402
Q

DPP-4 inhibitors

A

-gliptin
Blocks Dpp-4 enzyme slowing breakdown of GLP-1 increasing GLP-1.
Stimulates insulin release
NO effect on gastric emptying or satiety

403
Q

Biguanide

A

Metformin
Decreases hepatic production of glucose
Decreases glucose absorption in gut.
Increases insulin sensitivity in muscle and fat.
Increases glucose uptake.
Take with food.

404
Q

Biguanide (metformin) box warning

A

Metformin decreases hepatic uptake of lactate so lactic acidosis happens

405
Q

Thiazolidinediones

A

-glitazone
Decrease hepatic glucose
Lowers tricglyceride
Increases HDL
Activate nuclear receptor causing expression of genes that code for glucose and lipid metabolism.
Box warning - CHF
Avoid in youth

406
Q

SGLT2 inhibitors

A

-gliflozin
Increase renal excretion of glucose
Blocks SGLT-2 in PCT preventing glucose reabsorption causing glucose to be pissed out decreasing blood sugar
Can reduce CKD
Weight loss

407
Q

Why do thyroid meds take so long to take effect

A

Act on DNA in nucleus

408
Q

When should someone take thyroid meds

A

30 mins before first consumption of the day.
Need empty stomach

409
Q

Levothyroxine

A

Synthetic T4
Stable
Cheap
No allergenic foreign proteins
Must be converted to T3 in body

410
Q

Liothyronine

A

Synthetic T3
much more potent than levothyroxine.
Short half life so more doses.
Can easily put person into cardiotoxicity
Good for rapid onset or rapid termination

411
Q

Desiccated thyroid

A

Natural pork thyroid
T4 and T3 in 4:1 ratio
Commonly recalled

412
Q

Thioamides

A

Treat Hyperthyroidism
Prevent/interfere with hormone SYNTHESIS by inhibiting thyroid peroxidase.
Methimazole
Propylthiouracil
FDA pregnancy category D, but hyperthyroidism is also bad for pregnancy

413
Q

Propylthiouracil (PTU)

A

Thioamide
Preferred in first trimester of preg
Box warning of severe hepatitis

414
Q

Methimazole

A

Thioamide
More potent than PTU

PAS 506 (9 decks)

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